Course Videos
What was the physiological, safety, and compliance-focused rationale for combining basal insulin plus GLP-1 RA into a fixed ratio formulation? How would this approach achieve pan-glycemic (FBG and PPG) control?
From practical perspective, where are combination insulin-plus-GLP-1 RA regimens likely to fit into the sequencing algorithm for care of patients with T2D?
How do slow dose titration strategies for the fixed ratio, combination formulations, i.e. glargine insulin plus lixisenatide (iGlarLixi) vs. degludec insulin plus liraglutide (iDegLira) potentially affect the side effects seen?
What is your current perspective on the LEADER Trial and how should we translate its findings to the front lines of diabetes care? Can you describe the trial design?
What insights have we gained about drug-based management of the diabetic heart?
What insights have we gained about drug-based management of the diabetic heart?
From a translational perspective, who are the ideal patient candidates for the fixed ratio, combination formulations, i.e. glargine insulin plus lixisenatide (iGlarLixi) vs. degludec insulin plus liraglutide (iDegLira)?
Are there significant clinical differences—pharmacokinetic, safety, degree of weight loss, control of PPG—between the two combination formulations, i.e. glargine insulin plus lixisenatide (iGlarLixi) vs. degludec insulin plus liraglutide (iDegLira)?
Why do clinicians managing patients with T2D need to be aware of the trials, physiologic basis, side effects and other dimensions of deploying fixed ratio, long-acting insulin-GLP-1 RA combination regimens?
What is the rationale of combining GLP-1 RAs and long-acting insulin into fixed ratio combination agents?
Within the class of GLP-1 RAs, are there important comparative distinctions—dosing, PK/PD, side effects, weight loss, lipid profiles, and BP—that have clinical relevance that you believe should be highlighted? How do they differentially affect PPG?
What attributes—mechanistically, metabolically, and physiologically—of GLP-1 RAs, in your mind, support their position as foundational agents across a broad spectrum of patients with T2D?
For what reasons does insulin remain a foundational therapy for managing patients with T2D? And why does the addition of a GLP-1 RA potentially augment the utility of insulin-based management?